by Dan Roberts
February 2008
CD36 is a protein molecule (called an “integral membrane protein”) permanently attached to the surface of certain human cells. It plays a role in the inflammation process, but researchers have now discovered that a deficiency of the protein may cause the dry form of macular degeneration.
Researchers reported that deficiency of CD36 in rodent models led to significant progressive age-related photoreceptor degeneration. They think this is caused by a resulting down-regulation of COX2, an enzyme that is important to blood vessel formation. Uncontrolled blood vessel growth (neovascularization) is a hazard to the retina, as in wet AMD. A decrease, however, in the normal size and number of choroidal vessels will starve the photoreceptor cells, causing the dry form of the disease.
This discovery may lead to a treatment for CD36 deficiency, which could have important implications for the development of new therapies for dry AMD. The research was published on February 19, 2008 in PLoS Medicine (“CD36 Deficiency Leads to Choroidal Involution via COX2 Down-Regulation in Rodents,” Florian Sennlaub, et al, INSERM, Universite Pierre et Marie Curie, Paris).
